Evidence map›Paper›PMID 22740727›Full record

ReviewTexas Heart Institute journal2012

After avandia: the use of antidiabetic drugs in patients with heart failure.

Khaled I Khalaf, Heinrich Taegtmeyer

Open access · greenAbstract readReview
In one paragraph

Review in Texas Heart Institute journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. The Use of SGLT-2 Inhibitors in Type 2 Diabetes and Heart Failure.Metabolic syndrome and related disorders · 2015
    Review
  12. Article
  13. Article
  14. Complications of diabetes therapy.Endocrinology and metabolism clinics of North America · 2013
    Review
  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Khaled I KhalafDepartment of Internal Medicine, Division of Cardiology, University of Texas Medical School at Houston, Houston, Texas 77030, USA.
Heinrich Taegtmeyer
Texas Medical Center · US

Funding

SWITCHING OF METABOLIC GENES IN UNLOADED HEARTR01HL061483 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI TAEGTMEYER, HEINRICH · 1999 to 2021
$6.2M
Glucolipotoxicity and Cardiac Dysfunction in ObesityR01HL073162 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI TAEGTMEYER, HEINRICH · 2003 to 2007
$2.5M
NHLBI NIH HHS HL061483NHLBI NIH HHS HL073162NHLBI NIH HHS R01 HL061483NHLBI NIH HHS R01 HL073162
6 · The paper itself

Abstract

Managing diabetes mellitus is an ongoing concern, especially in the presence of heart failure. Recent reports have drawn attention to adverse cardiovascular events associated with the use of thiazolidinediones, including rosiglitazone (Avandia). In 2011, the U.S. Food and Drug Administration implemented a stringent "restricted access program" for the prescription of Avandia. Other studies, which have revealed increased mortality rates in association with tight glycemic control, raise serious concerns about managing diabetes in heart-failure patients. Herein, we provide a perspective on the management of noninsulin-dependent diabetes in patients with heart failure. We point out that thiazolidinediones exert their major effects through insulin sensitization, which potentiates the action of insulin. A defining feature of insulin resistance is excess fuel supply and restricted rates of substrate utilization by the heart. We postulate that the use of excess insulin and insulin-sensitizing agents can lead to adverse cardiovascular events and contractile dysfunction through an increase of substrate uptake to an insulin-resistant heart that is already flooded with fuel. We include a table of antidiabetic agents and nonpharmacologic interventions aimed at lowering substrate supply, and of the respective clinical trials supporting their safety and efficacy. Although previously contraindicated in patients with heart failure, metformin appears to be both safe and effective therapy for diabetes in those patients. Because metformin reduces gluconeogenesis in the liver, we propose that the management of diabetes in heart-failure patients should target the source, rather than the destination, of excess fuel.

Indexed as

Blood GlucoseComorbidityDiabetes Mellitus, Type 2GluconeogenesisGlycated HemoglobinHeart FailureHumansHypoglycemic AgentsInsulin ResistanceLiverMyocardiumRisk AssessmentRisk FactorsRosiglitazoneThiazolidinedionesTreatment OutcomeBlood GlucoseGlycated Hemoglobinhemoglobin A1c protein, humanHypoglycemic AgentsRosiglitazoneThiazolidinedionesCardiovascular diseases/mortality/prevention & controldiabetes mellitus, type 2/complications/drug therapy/mortalityheart failure, systolic/chemically inducedhypoglycemic agents/administration & dosageinsulin resistance/physiologymetformin/pharmacology/therapeutic userandomized controlled trials as topicrisk assessmentrosiglitazonethiazolidinediones/adverse effects

Identifiers

PMID22740727
PMCPMC3384032
OpenAlexW1543261695

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.